Random Records

Paper: Tumor suppressor RecQL5 controls recombination induced by DNA crosslinking agents doi: 10.1016/j.bbamcr.2014.01.005. Epub 2014 Jan 10 It is a little bit complicated to imagine how RecQL5 repairs the damage from interstrand crosslink (ICL) agent, like in this case cisplatin and mitomycin C. RecQ-family; DNA helicase (denature DNA duplex) - maintenance genome stability Focus on RecQL5 - RecQL5 - tumor suppressor - interact with Rad51- displace Rad51-ssDNA Gap; Precise role of RecQL5 is elusive. Results; 1.RecQL5 is involved in DNA interstrand crosslink (cisplatin, mitomycin C) repair. 2.Phenotype of RecQL5 KO resembled to FA gene KO cells 3.RecQL5 is involved in FANCD1 (BRCA2)-dependent ICL repair 4. Disappear of Rad51-foci delayed in REQL5KO cells after MMC treatment 5. Rad54 delayed Rad51-ssDNA in HR, compare to RecQL5 6.RecQL5 sensitivity to CDDP, and delayed Rad51-ssDNA detachment. 7.RecQL5 and Rad54 have a different effect on Rad51-ssDNA det...

I have read the news and view in the nature which summarizes two articles demonstrating the tumor cells, esp. lung adenocarcinomas (advanced and aggressive stage) divided and gave rise to two cell populations. ( doi :10.1038/nature22494) 1. tumour cells - actively dividing cells 2. supporting cell or so called "niche cell" - which provide the microenvironment to support the growth of the tumour cells Picture indicates the tumour cell divides and gives rise to two subpopulations (a). Within the tumour tissue, there are two cell subpopulations, one support the growth of tumour by which it secretes the growth factor that can stimulate the tumour cell growth (b). Question remains; supporting cell can secrete and promote the cancer growth in the other cancer type besides the its own neighbouring cells

Paper: Targeting DNA Repair in Cancer: Beyond PARP Inhibitors (doi: 10.1158/2159-8290.CD-16-0860) There are two main concepts for the DNA repair targeting, as far as I have observed; 1. if using as the monotherapy, then we have to understand the genotype of tumor cells; which mutation signature that causes tumor cells remain "the particular DNA repair mechanism". 2. if using as adjuvant therapy, it means administrated as the combination with the current cytotoxic drugs, and observe the genotype of cancer cells --> which DNA repair pathway predominantly used by the tumor cells and target that. Genetic signature of cancer cells is very important to use a tool to predict the therapeutic treatment choice. --- Here comes to what I want to make a note from this paper. DNA damage response; 1. how cell sense the damage 2. how cell sense the signal 3. how cell activate the cell cycle checkpoint 4. how cell trigger apoptosis 5. how cell orchestrates to initiate DNA ...

My friend has just sent me this paper and I have just finished skim through it. This is the note for myself on paper (it is quite fun to read and get the ideas both from the paper and from my friend); Paper -- Improved prediction of PARP inhibitor response and identification of synergizing agents through use of a novel gene expression signature generation algorithm (doi:  10.1038/s41540-017-0011-6). The team used two different databases to generate the algorithm ( iterative resampling analysis to predict sensitivity -- IRAPS) 1. Cancer cell line encyclopedia (focus on solid tumor cell line) --> contains the genotypic as well as gene expression profile of each cancer cell line 2. Genomics of drug sensitivity --> shows the relationship between the mutational status of cancer cells that are sensitive to particular drugs After generating the algorithm, they used theirs to test with the available cohort, in this case, cisplatin treatment which lacks a good responsive ma...

Paper: The crosstalk between Wnt/beta-catenin signaling pathway with DNA damage response and oxidative stress: Implications in cancer therapy (doi:10.1016/j.dnarep.2017.01.003) Before that we thought wnt signaling might not be related to DNA repair pathway, at all. Then we find this paper writing the review of wnt signaling contributing to DNA damage response and a bit of DNA repair. wnt signaling: 1. control gene expression 2 cell polarity 3. cell adhesion 4. cell behavior 5. DNA damage response --- Oxidative stress affect the wnt signaling, oxidative stress can cause the DNA lesion --- scope of this paper; review on the crosstalk of DDR, DNA repair, cellular activities through the wnt signaling pw. DDR: 1. sense the damage 2. transduce the signal to effector 3. determine the cell fate; cell cycle, fix, or death wnt signaling 1. determine the cell fate 1.1 cell proliferation 1.2  apoptosis 2. induce DDR through various protein 2.1 H2Ax 2.2 p16-INK4...

Paper: RNF43 (doi: 10.1136/jclinpath-2017-204763) Gene of the month in the journal of clinical pathology Only point out the detail I am interested Abstract; RNF43 1.function as tumor suppressor 2.negative feedback to wnt/beta-catenin 3.no RNF43 - no degradation of Frizzled and enhance the wnt/b-catenin signaling pw Introduction part; ZNRF3 -- Zinc And Ring Finger 3 --moderate identity 39% with RNF43 Profile Human RNF43; chromosome 17q23.2 11 exons - spanning 60 kb RNF43 proteins -- 2 isoforms 1. isoform 1 has 2 variants (shorter and longer) - different in mRNA strands but encoding the same protein 2. isoform 2 has shorter N-ter compare to isoform1 3. 783AA -- 90kDa RNF43 protein domains; 1. signal peptide 2. PA - protease-associated domain 2.1 PA -- putative protein recognition domain in distinctive set of TM ubiquitin ligase 2.2 function endocytic pw and cell surface PA domain of RN43 requires Dishevelled as adaptor to bind with Friz...

I have been confused with these three all the times and tend to forget pretty easily - so I need to write up with my own hand-writing with the good fountain pen. Homolog -- the origin (ancestral gene) Speciation -- ortho- Duplication (same species) -- para- I think computer algorithms would enable us to answer which gene is originated from which gene. There should be the pattern where the mathematics calculation could be solved and the factors from the environment to demonstrate the relationship.

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